Dysfunction of Ib (Autogenic) spinal inhibition in patients with progressive supranuclear palsy
Identifieur interne : 002F61 ( Istex/Corpus ); précédent : 002F60; suivant : 002F62Dysfunction of Ib (Autogenic) spinal inhibition in patients with progressive supranuclear palsy
Auteurs : Fine ; Mark Hallett ; Irene Litvan ; Nancy Tresser ; David KatzSource :
- Movement Disorders [ 0885-3185 ] ; 1998-07.
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- KwdEn :
Abstract
We compared the activity of Ib spinal interneurons in five patients with progressive supranuclear palsy (PSP) with six age‐matched control subjects. Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. The corticospinal pathways, unopposed by the medullary reticulospinal tract, may excessively activate Ib internurons.
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DOI: 10.1002/mds.870130410
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ISTEX:6336812FC761A9CBA44CD8E53FCEEA17F77C8537Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-07">1998-07</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="668">668</biblScope><biblScope unit="page" to="672">672</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">6336812FC761A9CBA44CD8E53FCEEA17F77C8537</idno><idno type="DOI">10.1002/mds.870130410</idno><idno type="ArticleID">MDS870130410</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autogenic inhibition</term><term>H reflex</term><term>Ia afferent</term><term>Ib interneurons</term><term>Progressive supranuclear palsy</term><term>Rigidity</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We compared the activity of Ib spinal interneurons in five patients with progressive supranuclear palsy (PSP) with six age‐matched control subjects. Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. The corticospinal pathways, unopposed by the medullary reticulospinal tract, may excessively activate Ib internurons.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Fine MD</name><affiliations><json:string>Neurology Service, Department of Veterans' Affairs Medical Center, and Department of Neurology, State University of New York at Buffalo, New York</json:string></affiliations></json:item><json:item><name>Mark Hallett MD</name><affiliations><json:string>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</json:string></affiliations></json:item><json:item><name>Irene Litvan MD</name><affiliations><json:string>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</json:string></affiliations></json:item><json:item><name>Nancy Tresser MD</name><affiliations><json:string>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</json:string></affiliations></json:item><json:item><name>David Katz MD</name><affiliations><json:string>Department of Pathology and Laboratory Medicine, Hartford Hospital, Hartford, Connecticut, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Progressive supranuclear palsy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Ib interneurons</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Autogenic inhibition</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Ia afferent</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Rigidity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>H reflex</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We compared the activity of Ib spinal interneurons in five patients with progressive supranuclear palsy (PSP) with six age‐matched control subjects. Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-07"></date><biblScope unit="vol">13</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="668">668</biblScope><biblScope unit="page" to="672">672</biblScope></imprint></monogr><idno type="istex">6336812FC761A9CBA44CD8E53FCEEA17F77C8537</idno><idno type="DOI">10.1002/mds.870130410</idno><idno type="ArticleID">MDS870130410</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We compared the activity of Ib spinal interneurons in five patients with progressive supranuclear palsy (PSP) with six age‐matched control subjects. Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. The corticospinal pathways, unopposed by the medullary reticulospinal tract, may excessively activate Ib internurons.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Progressive supranuclear palsy</term></item><item><term>Ib interneurons</term></item><item><term>Autogenic inhibition</term></item><item><term>Ia afferent</term></item><item><term>Rigidity</term></item><item><term>H reflex</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-10-02">Received</change><change when="1998-03-05">Registration</change><change when="1998-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6336812FC761A9CBA44CD8E53FCEEA17F77C8537/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. The corticospinal pathways, unopposed by the medullary reticulospinal tract, may excessively activate Ib internurons.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Dysfunction of Ib (Autogenic) spinal inhibition in patients with progressive supranuclear palsy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Ib INHIBITION PSP</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dysfunction of Ib (Autogenic) spinal inhibition in patients with progressive supranuclear palsy</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Fine</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Service, Department of Veterans' Affairs Medical Center, and Department of Neurology, State University of New York at Buffalo, New York</affiliation><description>Correspondence: Neurology Service, VA Medical Center, 3495 Bailey Ave., Buffalo, NY 14215, U.S.A.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Hallett</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Irene</namePart><namePart type="family">Litvan</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nancy</namePart><namePart type="family">Tresser</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Katz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology and Laboratory Medicine, Hartford Hospital, Hartford, Connecticut, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-07</dateIssued><dateCaptured encoding="w3cdtf">1997-10-02</dateCaptured><dateValid encoding="w3cdtf">1998-03-05</dateValid><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">22</extent></physicalDescription><abstract lang="en">We compared the activity of Ib spinal interneurons in five patients with progressive supranuclear palsy (PSP) with six age‐matched control subjects. Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. The corticospinal pathways, unopposed by the medullary reticulospinal tract, may excessively activate Ib internurons.</abstract><subject lang="en"><genre>Keywords</genre><topic>Progressive supranuclear palsy</topic><topic>Ib interneurons</topic><topic>Autogenic inhibition</topic><topic>Ia afferent</topic><topic>Rigidity</topic><topic>H reflex</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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